ArticleThe Journal of clinical investigation2019
ARHGEF1 deficiency reveals Gα13-associated GPCRs are critical regulators of human lymphocyte function.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
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- VerteBrain reveals novel neural and non-neural protein assemblies conserved across vertebrate evolution.bioRxiv : the preprint server for biology · 2025Article
- Platelet activation: a barrier to effective antitumor immunity.Cancer gene therapy · 2025Article
- Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury.Acta pharmaceutica Sinica. B · 2025Article
- GαFrontiers in cell and developmental biology · 2022Review
- B- and T-Cell Subset Abnormalities in Monogenic Common Variable Immunodeficiency.Frontiers in immunology · 2022Review
- GPCRs thatSmall GTPases · 2022Review
- Critical regulation of follicular helper T cell differentiation and function by GαProceedings of the National Academy of Sciences of the United States of America · 2021Article
- A homozygous stop-gain variant in ARHGAP42 is associated with childhood interstitial lung disease, systemic hypertension, and immunological findings.PLoS genetics · 2021Article
- Beyond monogenetic rare variants: tackling the low rate of genetic diagnoses in predominantly antibody deficiency.Cellular & molecular immunology · 2021Review
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3 authors at 1 institution in 1 country.
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Abstract
Primary antibody deficiencies are the most common immunodeficiencies in humans; however, identification of the underlying genetic and biochemical basis for these diseases is often difficult, given that these deficiencies typically involve complex genetic etiologies. In this issue of the JCI, Bouafia et al. performed whole-exome sequencing on a pair of siblings with primary antibody deficiencies and identified genetic mutations that result in a deficiency of ARHGEF1, a hematopoietic intracellular signaling molecule that transmits signals from GPCRs. ARHGEF1-deficient lymphocytes from the affected siblings exhibited important functional deficits that indicate that loss of ARHGEF1 accounts for the observed primary antibody deficiency, which manifests in an inability to mount antibody responses to vaccines and pathogens. Thus, this report demonstrates an important role for ARHGEF1 in GPCR signal transduction required for appropriate adaptive immune responses in humans.
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